Purpose of the Study:Mycobacterium tuberculosis secretes WXG100 proteins (100 amino
acids long containing a WXG motif) through a WXG100 secretion system (Wss) into the external
environment (1). WXG100 proteins signal to macrophages, for instance reducing cytokine
release and causing granuloma formation (2). The Wss is essential for the virulence of TB
(3,4).
A Wss has also recently been described in Staphylococcus aureus, where it is also vital for full
virulence of the organism (5). We sought to determine whether Streptococcus agalactiae (Group
B streptococcus; GBS) also encodes Wss and WXG100 proteins.

Experimental design: We BLAST searched each of the eight genes (SA0271-0278) encoding
the S. aureus Wss against the eight available GBS genomes. GBS genes were aligned to
determine conservation of a putative Wss across the GBS sequenced strains, and the wider
region was compared to define the genomic context.

Results: A putative Wss does exist in GBS (see Figure), and is conserved across the
sequenced strains. esxAB are WXG100 homologs, essA-C and esaA-C encode homologs of
proteins that are essential or accessory, respectively, to the function of the Wss in
S. aureus. GBS
genomes contain three WXG100 homologs, only one of which is associated with the Wss. The
Wss is located within the genome on a mobile segment of DNA, termed ‘Putative Pathogenicity
Island-IX’, implying that the Wss has been acquired by horizontal transfer. Similarly, the two
WXG100 genes that are not associated with the Wss are also located in Putative Pathogenicity
Islands -I and –XIII.

Conclusions and discussion: A Wss has not previously been recognised in GBS, but is
identified in this study. This finding enhances our knowledge of the potential mechanisms by
which GBS causes disease. It is now plausible that GBS also attenuates macrophages through the
action of a WXG100 homolog. In TB, the absence of the Wss is the main determinant of the
attenuation of BCG (4). Our finding of a putative Wss in GBS thus has implications for
attenuated GBS vaccine development.